Concomitant antitumor immunity to syngeneic tumors will be studied with the aim of characterizing the T cells that express it and the T cells that suppress it. The hypothesis will be tested that immunotherapy with immunoadjuvants represents an attempt to superimpose an augmented T cell-mediated immune response on an already ongoing concomitant immune response that undergoes T cell-mediated negative regulationbefore it causes regression of the tumor. Experiments will be designed to determine whether effector T cells differ from suppressor T cells with respect to sensitivity to cyclophosphamide, gamma-irradiation, and the antimitotic drug, vinblastine. Effector and suppressor T cells will be compared in terms of the kinetics of their generation, with a view to determining whether the onset of decay of the cyc=tolytic T cell response to progressive tumor growth coincides with the emergence of suppressor T cells that are capable of suppressing the generation of cytolytic T cells, as measured by in vivo and in vitro assays. It will determine whether tumor regression caused by cyclophosphamide or gamma irradiation partly depends on the ability of these agents to enhance concomitant immunity by preferentially eliminating suppressor T cells or their precursors. The therapeutic action of Corynebacterium parvum will be studied in terms of its ability to augment positive regulation of concomitant anti-tumor immunity, and in terms of its inability to overcome negative regulation of this immunity. Experiments will be performed to determine whether intravenously infused suppressor T cells can prevent, or interfere with C. parvum-induced tumor regression. It is postulated that suppressor T cells will prove to be the major obstacle to tumor immunotherapy.